Document Detail

The diastolic decay constant in spontaneously hypertensive rats versus WKY rats as an indicator for vasomotor control.
MedLine Citation:
PMID:  9188082     Owner:  NLM     Status:  MEDLINE    
This research uses the diastolic decay constant (tau) to investigate the short term mechanism responsible for vasomotor control, mainly the alpha-sympathetic control system. Previous studies have shown that vasomotor control is altered in spontaneously hypertensive rats (SHR) preceding the phase of overt hypertension. The diastolic decay, according to the two element Windkessel model, displays an exponential shape with a decay constant, tau, depending on both the vascular resistance and the compliance. In our experiments, we used tau to characterize vasomotor activity and its control in the normotensive rats as well as in the spontaneously hypertensive rats (SHR) prone to hypertension. The beat to beat value of tau was evaluated from a continuous arterial blood pressure (ABP) signal, measured in the tail artery of the conscious, unrestrained rat. Four months old prehypertensive SHR were compared to their age matched normotensive controls (WKY). To study vasomotor regulation, we computed gains and delay times by investigating the compensatory response in tau to changes in mean ABP (MBP). These parameters are expected in the short term to be neurally controlled by the sympathetic system, mainly alpha-sympathetic. Our set of experiments consisted of changing MBP by performing successive injections in bolus of increasing doses of the vasoconstrictor angiotensin II. This procedure was repeated under double cardiac autonomic blockade of the vagal and beta 1 = sympathetic limbs. Our results show that, under baseline conditions, the absolute gain and delay times of tau are reduced in SHR compared to WKY. Double cardiac blockade decreases the absolute gain in both strains, while abolishing the baseline strain differences. These results reinforce our assumption that, in SHR, the alpha-sympathetic system is in a basic state of excitation even prior to the onset of overt hypertension and therefore reacting with reduced sensitivity (lower gain) to changes in MBP.
S Eyal; O Oz; S Eliash; G Wasserman; S Akselrod
Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Journal of the autonomic nervous system     Volume:  64     ISSN:  0165-1838     ISO Abbreviation:  J. Auton. Nerv. Syst.     Publication Date:  1997 May 
Date Detail:
Created Date:  1997-08-11     Completed Date:  1997-08-11     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8003419     Medline TA:  J Auton Nerv Syst     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  24-32     Citation Subset:  IM    
Physics Department, Tel-Aviv University, Israel.
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MeSH Terms
Adrenergic beta-Antagonists / pharmacology
Autonomic Nerve Block
Heart Conduction System / drug effects,  physiopathology
Hypertension / physiopathology*
Nerve Block
Rats, Inbred SHR / physiology*
Rats, Inbred WKY / physiology
Reference Values
Time Factors
Vagus Nerve / physiopathology
Vasomotor System / physiopathology*
Reg. No./Substance:
0/Adrenergic beta-Antagonists

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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